Senescence is generally categorized into physiological senescence and pathological senescence. Physiological senescence inevitably occurs through aging and involves changes in hair, skin, eyes, bones, brain, etc. and reduction of motor function and energy metabolism. Recent years' studies have suggested that reduction of energy metabolism due to senescence is related to mitochondrial dysfunction such as mutation or damage of mitochondrial DNA (Non-Patent Document 1).
When muscle force and physical endurance are reduced through senescence, daily life activity is impaired. Also, reduction of energy metabolism and mitochondrial function causes unbalanced energy intake and consumption, possibly causing life-style-related diseases such as obesity and diabetes. In advanced countries, prevention of life-style-related diseases is an important target from the viewpoint of improvement of quality-of-life (QOL). Therefore, in order to improve QOL and prolong a healthy period of life, important factors are to prevent aging-related reduction of physiological function; i.e., senescence, and particularly to maintain physical endurance, suppress fatigue, maintain energy metabolism at a high level, and improve mitochondrial function.
Generally, muscular atrophy, which involves reduction in muscle mass and muscle force, includes disuse muscular atrophy, sarcopenia, etc. When muscular atrophy occurs, muscle function is reduced. Particularly in the case of an aged person, muscular atrophy and reduced muscle force due to senescence were observed, and muscle damage and fracture tend to occur. During a period of treatment and curing thereof under restriction of movement through rest or by means of a cast, disuse muscular atrophy and muscle dysfunction are accelerated. Aged people are readily involved in such a mal-cycle, and in the worst case bedridden. Therefore, in order to improve daily life functions, prolong a healthy period of life, and maintain quality-of-life (QOL), disuse muscular atrophy and muscle dysfunction are to be prevented through physical exercise of certain strength, to thereby maintain motor function and total body functions in a favorable state.
Senescence progresses by genetic and environmental factors and is considered to be retarded through improvement of environmental factors including those related to life style (e.g., diet or physical exercise). For preventing a decrease in motor performance or muscle function and muscular atrophy which accompany senescence, a repeated physical exercise with an appropriate strength during a healthy period, a physical rehabilitation therapy, etc. are effective means. Particularly in the case of an aged person, repeated physical exercise with an appropriate strength, physical rehabilitation therapy, etc. are effective. However, since such exercises may involve possible injuries or encounter difficulty in maintenance of motivation, there is demand for safer and more effective prevention means.
Some components which can suppress physical senescence have already been known. For example, there have been disclosed an anti-aging composition containing a bio-collagen synthesis promoter and an abnormal protein remover as an skin senescence inhibition component (Patent Document 1), an anti-aging agent containing a carrot leaf extract as an effective ingredient (Patent Document 2), and an anti-aging composition containing a Japanese horseradish (wasabi) extract and a rush extract as an essential ingredient (Patent Document 3).
Also disclosed are the following: a cell senescence inhibitor containing a Mannen-take solvent extract as a telomere shortening suppression component (Patent Document 4), and cacao and/or cacao mass (Patent Document 5), an organic germanium compound (Patent Document 6) and L-arginine, phosphatidylserine, docosahexanoic acid, ginkgo leaves or ginkgo leaf extract, and tocopherol (Patent Document 7), as a brain senescence inhibitor. Also disclosed is an L-arginine-containing preventive/therapeutic composition for the onset of clinical symptoms in a disease caused by mitochondrial function abnormality (Patent Document 8).
In addition to physical exercises and physical therapy, screening of components for preventing muscular atrophy, muscle dysfunction associated with muscular atrophy, and a bedridden state has been carried out through nutritional approaches. For example, the following are disclosed: senescence inhibition by cystine and theanine (Patent Document 9), muscular atrophy inhibition by fruit-derived polyphenol (Patent Document 10), muscular protein degradation inhibition by lycopene (Patent Document 11), inhibition of decrease in motor performance by an organic acid having 2 or more carboxyl groups or a salt thereof as an active ingredient (Patent Document 12), astaxanthin and/or an ester thereof as a fatigue-preventing agent (Patent Document 13), proanthocyanidine serving as a muscular atrophy inhibitor and motor function improving agent (Patent Documents 14 and 15), and relaxation of oxidative stress of muscle by superoxide dismutase (Patent Document 16). However, at present, studies have not yet been conducted on the actual effects on reduction of muscle force and muscular atrophy accompanying aging.
Meanwhile, physiologically useful properties of catechins contained in green tea, black tea, cacao beans, etc. have already been reported. For example, cholesterol level increase suppression action (Patent Document 17), blood sugar level increase suppression action (Patent Document 18), arteriosclerosis prevention action (Patent Document 19), physical endurance improving action (Patent Document 20), and muscular dystrophy suppression action (Non-Patent Document 2) are reported.
However, hitherto, any inhibitory actions of catechin on senescence and mitochondrial function, particularly decrease in physical endurance and energy metabolism, fatigue, and dysfunction of mitochondria, have not been known.
Actions of catechin on disuse muscular atrophy and muscle dysfunction associated therewith have also not been reported.
Meanwhile, leucine, valine, and isoleucine, which are branched-chain amino acids, are known as useful agents: an impaired glucose tolerance treatment agent (Patent Document 21), an agent for maintaining instantaneous power and endurance of muscle (Patent Document 22), and a muscle pain and stiffness reliever (Patent Document 23). Among them, leucine is reported to have an insulin secretion promoting action (Non-Patent Document 3), a muscular protein synthesis action (Non-Patent Document 4), etc. However, the actions of catechins, amino acids, and a combination thereof on an inhibitory action on decrease in muscle weight and muscle force accompanying senescence have not been known.
Patent Document 1: JP-A-2004-115438
Patent Document 2: JP-A-2004-51580
Patent Document 3: JP-A-2006-63038
Patent Document 4: JP-A-2003-12539
Patent Document 5: JP-A-2005-281285
Patent Document 6: JP-A-H11-43432
Patent Document 7: JP-A-2003-261456
Patent Document 8: JP-A-2004-182705
Patent Document 9: WO 2005-123058, pamphlet
Patent Document 10: JP-A-2001-89387
Patent Document 11: JP-A-2004-59518
Patent Document 12: JP-A-H10-17585
Patent Document 13: JP-A-2006-16409
Patent Document 14: JP-A-2002-338464
Patent Document 15: JP-A-2005-97273
Patent Document 16: JP-A-2006-62976
Patent Document 17: JP-A-S60-156614
Patent Document 18: JP-A-H4-253918
Patent Document 19: JP-A-H4-352726
Patent Document 20: JP-A-2005-89384
Patent Document 21: JP-A-2006-28194
Patent Document 22: JP-A-2000-26290
Patent Document 23: JP-A-2000-26289
Non-Patent Document 1: Iwanami Lectures, Gendai Igaku no Kiso (“Basic Modern Medicine”), vol. 12, No. 2, pp. 55-58, 1999
Non-Patent Document 2: Dorchies O. M. et al, AJP-Cell Physiol., vol. 290, No. 2, pp. 616-25, 2006
Non-Patent Document 3: Brouwer A. E. et al, Pancreas, vol. 6, No. 2, pp. 221-8, 1991
Non-Patent Document 4: Crozier S. J. et al, J. Nutr., vol. 135, No. 3, pp. 376-82, 2005